Fucoidan could regulate the inflammation response via HMGB1 and NF-κB inactivation in I/R-induced myocardial damage. - GreenMedInfo Summary

The aim of the study was to determine the effects of fucoidan on rat myocardial ischemia-reperfusion (I/R) model and elucidate the potential mechanisms. Myocardial I/R injury was induced by the occlusion of left anterior descending coronary artery for 30 min followed by reperfusion for 2h. After 2h reperfusion, hemodynamics parameters were detected. Blood samples were collected to determine serum levels of tumor necrosis factor-α (TNF-α) and interleukin 6, 10 (IL-6, 10). Hearts were harvested to assess histopathological changes, infarct size (IS), and the content of myeloperoxidase (MPO). The expression of high-mobility group box 1 (HMGB1), phosphor-IκB-α and phosphor-nuclear factor kappa B (NF-κB) were assayed by western blot. Compared with control group, treatment with fucoidan improved left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP) and the contractility index (P<0.05, P<0.01). Fucoidan reduced the myocardial IS, the levels of TNF-α and IL-6, and the activity of MPO (P<0.05, P<0.01). Fucoidan down-regulated the expression of HMGB1, phosphor-IκB-α and NF-κB, but increased the content of IL-10 when compared with control (P<0.05, P<0.01). Besides, the infiltration of polymorph nuclear leukocytes (PMNs) and histopathological damages in myocardium were decreased in fucoidan treated groups (PMNs, P<0.05, P<0.01). These findings revealed that the administration of fucoidan could regulate the inflammation response via HMGB1 and NF-κB inactivation in I/R-induced myocardial damage.